I understand that high fructose corn syrup was found to have detrimental effects on peoples' health. Why is this so?
Besides a lot of propaganda there is not much evidence that high fructose corn syrup (HFCS) is more dangerous than normal sugar. Lets have a look at the sugar in detail:
HFCS is produced from corn and is originally a glucose syrup. Since fructose is obviously much sweeter, the glucose is converted enzymatically into fructose (see here for more details). Before the use in food production additional glucose is added to the syrup so that typical syrups contain 55% fructose and 42% glucose or 42% fructose and 53% glucose (the remaining % are water).
If you look at saccharose (which is our ordinary sugar) then this is a disaccherid which is build from one molecule of glucose and one molecule of fructose. The enzyme sucrase breaks this molecule up into one molecule of fructose and glucose each, so reaching a 50%:50% ratio between the sugars.
As the ratios are more or less the same, it doesn't matter for the human body, where the sugar come from meaning that in this context it is more too much sugar in the food than a problem with HFCS, as also this study suggests:
Fructose itself is not without problems as this induces the production of fats in the liver, but again, it doesn't matter for the body, where this fructose comes from:
For further reading I can also recommend this article on Gizmodo:
The following study abstract of "Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity" copied from http://www.ncbi.nlm.nih.gov/pubmed/15051594 seems to address your question. I added a paragraph break; the second paragraph seems most relevant to me:
Obesity is a major epidemic, but its causes are still unclear. In this article, we investigate the relation between the intake of high-fructose corn syrup (HFCS) and the development of obesity. We analyzed food consumption patterns by using US Department of Agriculture food consumption tables from 1967 to 2000. The consumption of HFCS increased > 1000% between 1970 and 1990, far exceeding the changes in intake of any other food or food group. HFCS now represents 40% of caloric sweeteners added to foods and beverages and is the sole caloric sweetener in soft drinks in the United States. Our most conservative estimate of the consumption of HFCS indicates a daily average of 132 kcal for all Americans aged > or = 2 y, and the top 20% of consumers of caloric sweeteners ingest 316 kcal from HFCS/d.
The increased use of HFCS in the United States mirrors the rapid increase in obesity. The digestion, absorption, and metabolism of fructose differ from those of glucose. Hepatic metabolism of fructose favors de novo lipogenesis. In addition, unlike glucose, fructose does not stimulate insulin secretion or enhance leptin production. Because insulin and leptin act as key afferent signals in the regulation of food intake and body weight, this suggests that dietary fructose may contribute to increased energy intake and weight gain. Furthermore, calorically sweetened beverages may enhance caloric overconsumption. Thus, the increase in consumption of HFCS has a temporal relation to the epidemic of obesity, and the overconsumption of HFCS in calorically sweetened beverages may play a role in the epidemic of obesity.
Fructose has a special characteristic that other sugars do not have: its absorption in the human intestine is not regulated, as opposed to glucose, for example.
The important implication is that all the fructose you consume will end inside your organism, either used immediately or stored as fat. Other sugars will only be partly assimilated, or will require more energy to assimilate. If you take the example of glucose again, a glucose molecule requires active transport (meaning consumes ATP, the most basic fuel of your organism) to transit across the intestinal wall. Fructose is absorbed via free transport (i.e. no ATP consumption).
This claim can be verified by opening any human physiology book, and while it is debatable whether fructose itself is deleterious, increasing the sugar amount in an already sugar-saturated environment clearly does not seem a good idea to me.
I (inf3rno) appended the answer with further details:
Sucrose is split by digestive enzymes (sucrase, glycoside hydrolase) in the small intestine into fructose and glucose (1:1 ratio). By the high fructose corn syrup (HFCS hereafter) the fructose - glucose ratio is dependent on the HFCS type according to wikipedia. For example HFCS90 has 90% fructose, while HFCS42 has only 42% fructose (the rest is glucose).
Glucose is mainly transported by SGLT1 (active transport, which involves ATP), while fructose is mainly transported by GLUT5 (passive transport, does not involve ATP) into enterocytes in the intestines. After that the cells transport these sugars with GLUT2 (passive transport, not insulin dependent) into the blood. Fructose and glucose is transported to the liver (hepatocytes) from the blood, with GLUT2.
In the liver fructose is more dangerous than glucose, because it is transformed without any regulation. It uses the same pathways as glucose and mostly fatty acids are created from it, which increase the blood VLDL, LDL, FFA level and cause insulin resistance. The byproducts are urate and free radicals, which cause hyperuricaemia and oxidative stress. Hyperuricaemia cause decreased NO levels (by counteracting with eNOS and reacting with NO directly), which cause increased blood pressure due to vasoconstriction. Hyperuricaemia damages the liver and the kidney too. Too high urate levels enhance LDL oxidation as well, which cause atherosclerosis. The free radicals deplete the antioxidants of the body and probably cause cancer in long term.
- High dietary fructose intake: Sweet or bitter life? - http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3158875/
- A causal role for uric acid in fructose-induced metabolic syndrome - http://ajprenal.physiology.org/content/290/3/F625
- Gut microbial adaptation to dietary consumption of fructose, artificial sweeteners and sugar alcohols: implications for host–microbe interactions contributing to obesity - http://www.drperlmutter.com/wp-content/uploads/2014/04/Payne-et-al-2012-Obesity-reviews.pdf
- Early Life Exposure to Fructose and Offspring Phenotype: Implications for Long Term Metabolic Homeostasis - http://dx.doi.org/10.1155/2014/203474
- Dietary fructose, salt absorption and hypertension in metabolic syndrome: towards a new paradigm - http://onlinelibrary.wiley.com/doi/10.1111/j.1748-1716.2010.02167.x/abstract?deniedAccessCustomisedMessage=&userIsAuthenticated=false
- Toward a Unifying Hypothesis of Metabolic Syndrome - http://pediatrics.aappublications.org/content/129/3/557.short
- Uric acid transport and disease - http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2877959/
@Chris: So summed up I think this is enough proof that HFCS with higher fructose - glucose ratio, than sucrose have a higher health risk.
protected by AliceD♦ Jan 30 '15 at 8:20
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